1. Godfrey, Jason, Riscal, Romain, Skuli, Nicolas, Simon, M Celeste. 2022. Glucagon signaling via supraphysiologic GCGR can reduce cell viability without stimulating gluconeogenic gene expression in liver cancer cells. In Cancer & metabolism, 10, 4. doi:10.1186/s40170-022-00280-1. https://pubmed.ncbi.nlm.nih.gov/35123542/
2. Liu, Qiaofeng, Lin, Guangyao, Chen, Yan, Yang, Dehua, Wang, Ming-Wei. . Deleterious mutation V369M in the mouse GCGR gene causes abnormal plasma amino acid levels indicative of a possible liver-α-cell axis. In Bioscience reports, 41, . doi:10.1042/BSR20210758. https://pubmed.ncbi.nlm.nih.gov/34002801/
3. Monfeuga, Thomas, Norlin, Jenny, Bugge, Anne, Feigh, Michael, Holst, Dorte. 2023. Evaluation of long acting GLP1R/GCGR agonist in a DIO and biopsy-confirmed mouse model of NASH suggest a beneficial role of GLP-1/glucagon agonism in NASH patients. In Molecular metabolism, 79, 101850. doi:10.1016/j.molmet.2023.101850. https://pubmed.ncbi.nlm.nih.gov/38065435/
4. Thymiakou, Efstathia, Tzardi, Maria, Kardassis, Dimitris. 2022. Impaired hepatic glucose metabolism and liver-α-cell axis in mice with liver-specific ablation of the Hepatocyte Nuclear Factor 4α (Hnf4a) gene. In Metabolism: clinical and experimental, 139, 155371. doi:10.1016/j.metabol.2022.155371. https://pubmed.ncbi.nlm.nih.gov/36464036/